Yingyu Bai, Xiaoying Zhang, Ying Li, Fei Qi, Chong Liu, Xiaojie Ai, Mingxin Tang, Christopher Szeto, Erhe Gao, Xiang Hua, Mingxing Xie, Xuejun Wang, Ying Tian, Yongjie Chen, Guowei Huang, Junping Zhang, Weidong Xiao, Lili Zhang, Xueyuan Liu, Qing Yang, Steven R Houser, Xiongwen Chen
BACKGROUND: The sympathoadrenergic system and its major effector PKA (protein kinase A) are activated to maintain cardiac output coping with physiological or pathological stressors. If and how PKA plays a role in physiological cardiac hypertrophy (CH) and pathological CH (PaCH) are not clear. METHODS: Transgenic mouse models expressing a PKA inhibition peptide-GFP fusion protein in a cardiac-specific and inducible manner (cPKAi) were used to determine the roles of PKA in physiological CH during postnatal growth or induced by swimming, and in PaCH induced by transaortic constriction (TAC) or augmented Ca2+ influx...
January 26, 2024: Circulation Research